Calorie restriction improves whole-body glucose disposal and insulin resistance in association with the increased adipocyte-specific GLUT4 expression in Otsuka Long–Evans Tokushima Fatty rats

Park, Seung Yeon; Choi, Guem H.; Choi, Hyo I.; Ryu, Jiwon; Jung, Chan Y.; Lee, Wan

doi:10.1016/j.abb.2005.01.010

Cited by 59 publications

(42 citation statements)

References 51 publications

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“…One reason for this may be the lack of an adequate animal model exhibiting an age-dependent nonobese phenotype of type 2 diabetes. Previous animal models such as the ob/ob mouse and OLETF rat develop early-onset diabetes resembling obesity-dependent human diabetes, but not late-onset, non-obese type 2 diabetes [4,5]. We found that male offspring of non-diabetic C57BL/6 and DBA/2 mice, called here JYD mice, developed type 2 diabetes when they grew old.…”

Section: Introductionmentioning

confidence: 73%

A potential role for skeletal muscle caveolin-1 as an insulin sensitivity modulator in ageing-dependent non-obese type 2 diabetes: studies in a new mouse model

Khil

Cho

et al. 2008

Diabetologia

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Aims/hypothesis Type 2 diabetes mellitus is a common agedependent disease. We discovered that male offspring of non-diabetic C57BL/6 and DBA/2 mice, called JYD mice, develop type 2 diabetes when they grow old. JYD mice show characteristics of insulin resistance, hyperglycaemia and hyperinsulinaemia in old age without obesity. We postulated that the mechanism of age-dependent type 2 diabetes in this model relates to caveolin-1 status in skeletal muscle, which appears to regulate insulin sensitivity in the mice. Methods We compared insulin sensitivity in aged C57BL/6 and JYD mice using glucose and insulin tolerance tests and 18 Ffluorodeoxyglucose positron emission tomography. We also determined insulin signalling molecules and caveolin proteins using western blotting, and altered caveolin-1 levels in skeletal muscle of C57BL/6 and JYD mice using viral vector systems, to examine the effect of this on insulin sensitivity. Results In 30-week-old C57BL/6 and JYD mice, the basal levels of IRS-1, Akt and peroxisome proliferator-activated receptor-γ decreased, as did insulin-stimulated phosphorylation of Akt and insulin receptor β. However, caveolin-1 was only increased about twofold in 30-week-old JYD mice as compared with 3-week-old mice, whereas an eightfold increase was seen in C57BL/6 mice. Downregulation of caveolin-1 production in C57BL/6 mice caused severe impairment of glucose and insulin tolerance. Upregulation of caveolin-1 in aged diabetic JYD mice significantly improved insulin sensitivity with a concomitant increase of glucose uptake in the skeletal muscle. Conclusions/interpretation The level of skeletal muscle caveolin-1 is correlated with the progression of age-dependent type 2 diabetes in JYD mice.

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Section: Introductionmentioning

confidence: 73%

A potential role for skeletal muscle caveolin-1 as an insulin sensitivity modulator in ageing-dependent non-obese type 2 diabetes: studies in a new mouse model

Khil

Cho

et al. 2008

Diabetologia

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“…For example, 40% caloric restriction reversed insulin resistance in pinealectomized rats by enhancing GLUT4 content in adipocytes and its translocation to the plasma membranes (Zanquetta et al 2003). Similarly in fatty rats caloric restriction improved glucose utilization by upreguletion of adipocyte GLUT4 expression (Park et al 2005). Under the conditions of clinically manifested AA the loss of appetite occurs, that is manifested by reduced food consumption by about 40%, and consequently by body and fat mass loss (Stofkova et al 2009).…”

Section: Discussionmentioning

confidence: 99%

Alterations in adipocyte glucose transporter GLUT4 and circulating adiponectin and visfatin in rat adjuvant induced arthritis

Jurčovičová¹,

Štofková²,

Škurlová³

et al. 2010

gpb

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Abstract. Rheumatoid arthritis in humans brings about impaired insulin sensitivity and glucose tolerance. Since adipose tissue plays a role in glucose homeostasis, we evaluated the size of adipocytes, the amount of glucose transporter type 4 (GLUT4) in adipocyte plasma membranes, and circulating insulin, glucose, and adipokines affecting glucose metabolism, resistin, adiponectin and visfatin during experimental adjuvant arthritis (AA) in male Lewis rats. AA was induced by a single injection of complete Freund's adjuvans. Adipocyte diameter was assessed microscopically, GLUT4 was measured by Western blotting. Plasma insulin, adiponectin, visfatin were quantitated by RIA, and resistin by ELISA. Arthritic rats showed cachexia, reduced adipocyte size, and downregulated membrane GLUT4 (4065 ± 962 vs. 9911 ± 680 arb. units of optic density, p < 0.01), reduced plasma adiponectin (1.956 ± 0.10 vs. 3.16 ± 0.22 µg/ml, p < 0.001), and enhanced visfatin (1.84 ± 1.05 vs. 1.24 ± 0.1 ng/ml, p < 0.01). Plasma glucose and insulin were unaltered, as were the resistin levels. Conclusion: AA induced cachexia results in reduction of adipocyte size, and paradoxically also in downregulation of GLUT4 in adipocyte membranes. This is supposed to be functionally related to the reduced adiponectin levels. The upregulated visfatin in rat arthritis is a novel finding, and it confirms its role in autoimmunity across the species.

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“…It is possible that the effects of ALA treatment on whole body glucose tolerance are due to the anorexic effects of ALA, thereby reducing not only the triglyceride accumulation in the different fat depots but also targeting ectopic lipid accumulation. It is well known that moderate reduction in caloric intake, without causing malnutrition, is effective in obese diabetic rats to improve insulin stimulated glucose uptake and lower insulin levels during a GTT ( 28,29 ). ( 25,26 ).…”

Section: Discussionmentioning

confidence: 99%

Prevention of high-fat diet-induced muscular lipid accumulation in rats by α lipoic acid is not mediated by AMPK activation

Timmers

Bosch

Towler

et al. 2010

Journal of Lipid Research

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Obesity has reached epidemic proportions globally and the situation is likely to deteriorate further. It is well known that obesity predisposes individuals to a range of serious health complications with high morbidity rates including insulin resistance, type 2 diabetes mellitus, and cardiovascular diseases ( 1 ). The mechanisms underlying the progression from obesity to insulin resistance and, ultimately, type 2 diabetes are not fully elucidated ( 2 ). It is speculated that excessive FFA mobilization from adipose tissue leads to an increase in plasma FFA with ectopic deposition of triglycerides in muscle, the liver, and the pancreas as a result. The increased intramyocellular lipid (IMCL) content could disturb muscle insulin signaling, which ultimately results in muscle insulin resistance ( 3 ).Alpha lipoic acid (ALA), also known as thioctic acid, is a naturally occurring short-chain fatty acid with a powerful antioxidant capacity. It is synthesized in small amounts by plants and animals, including humans ( 4, 5 ). Endogenously synthesized ALA is an essential cofactor for several mitochondrial enzyme complexes that catalyze critical reactions related to energy production ( 6 ). ALA can also be exogenously derived from various food sources such as toAbstract Skeletal muscle triglyceride accumulation is associated with insulin resistance in obesity. Recently, it has been suggested that ␣ lipoic acid (ALA) improves insulin sensitivity by lowering triglyceride accumulation in nonadipose tissues via activation of skeletal muscle AMP-activated protein kinase (AMPK). We examined whether chronic ALA supplementation prevents muscular lipid accumulation that is associated with high-fat diets via activation of AMPK. In addition, we tested if ALA supplementation was able to improve insulin sensitivity in rats fed low-and high-fat diets (LFD, HFD). Supplementing male Wistar rats with 0.5% ALA for 8 weeks signifi cantly reduced body weight, both on LFD and HFD ( ؊ 24% LFD+ALA vs. LFD, P < 0.01, and ؊ 29% HFD+ALA vs. HFD, P < 0.001). Oil red O lipid staining revealed a 3-fold higher lipid content in skeletal muscle after HFD compared with LFD and ALA-supplemented groups ( P < 0.05). ALA improved whole body glucose tolerance ( ‫ف‬ 20% lower total area under the curve (AUC) in ALA supplemented groups vs. controls, P < 0.05). These effects were not mediated by increased muscular AMPK activation or ALA-induced improvement of muscular insulin sensitivity. To conclude, the prevention of HFD-induced muscular lipid accumulation and the improved whole body glucose tolerance are likely secondary effects due to the anorexic nature of ALA. -Timmers, S., J. Abbreviations: ACC, acetyl-CoA carboxylase; ALA, ␣ lipoic acid; AMPK, AMP-activated protein kinase; AUC, area under the curve; % E, % energy; HFD, high-fat diet; IMCL, intramyocellular lipid; IpGTT, intraperitoneal glucose tolerance test; LFD, low-fat diet; OLETF, Otsuka Long Evans Tokushima Fatty.

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Calorie restriction improves whole-body glucose disposal and insulin resistance in association with the increased adipocyte-specific GLUT4 expression in Otsuka Long–Evans Tokushima Fatty rats

Cited by 59 publications

References 51 publications

A potential role for skeletal muscle caveolin-1 as an insulin sensitivity modulator in ageing-dependent non-obese type 2 diabetes: studies in a new mouse model

A potential role for skeletal muscle caveolin-1 as an insulin sensitivity modulator in ageing-dependent non-obese type 2 diabetes: studies in a new mouse model

Alterations in adipocyte glucose transporter GLUT4 and circulating adiponectin and visfatin in rat adjuvant induced arthritis

Prevention of high-fat diet-induced muscular lipid accumulation in rats by α lipoic acid is not mediated by AMPK activation

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